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Advances in Virus Research 1972This chapter summarizes the experimental evidence bearing on the nature of virus-erythrocyte reactions characteristic of several taxonomic groups.. Such evidence is... (Review)
Review
This chapter summarizes the experimental evidence bearing on the nature of virus-erythrocyte reactions characteristic of several taxonomic groups.. Such evidence is culled from (1) the study of conditions necessary for hemagglutination; (2) the examination of specific factors affecting either the cell or the virion to enhance, alter, or abolish the reaction; and (3) the direct physicochemical analysis of cells, viruses, and “receptor analogs.” The hemadsorption phenomenon also provides evidence for virus-erythrocyte interactions, which is based on the attachment of erythrocytes to infected cells in culture having hemagglutinin at their surfaces. This phenomenon reflects the interaction between erythrocytes and viral envelope components. The major virus groups that react with erythrocytes include myxoviruses, paramyxoviruses, pseudomyxoviruses, adenoviruses, arboviruses, reoviruses, enteroviruses, and miscellaneous hemagglutinating viruse (rubella virus, coronaviruses, rhabdoviruses, and oncogenic viruses). The agglutination of erythrocytes by the direct action of viral particles was first described in connection with myxoviruses. This led directly to the discovery of viral neuraminidase—a property unique to myxoviruses and paramyxoviruses. A number of viruses unrelated to myxoviruses have since been shown to agglutinate erythrocytes of various species. The visible result of viral hemagglutination is the “pattern” formed at the bottom of a test tube or well plate by lattices of red cells lightly conjoined by viral hemagglutinin. Hemagglutination serves as a useful direct means of titering intact viral particles or hemagglutinating subunits.
Topics: Adenoviridae; Animals; Arboviruses; Butanols; Cell Membrane; Chickens; Enterovirus; Erythrocytes; Haplorhini; Hemadsorption; Hemagglutination; Humans; Oncogenic Viruses; Orthomyxoviridae; Paramyxoviridae; Rats; Reoviridae; Rubella virus; Viruses
PubMed: 4348510
DOI: 10.1016/s0065-3527(08)60746-0 -
Tumour Virus Research Dec 2022Human tumor viruses cause various human cancers that account for at least 15% of the global cancer burden. Among the currently identified human tumor viruses, two are... (Review)
Review
Human tumor viruses cause various human cancers that account for at least 15% of the global cancer burden. Among the currently identified human tumor viruses, two are small DNA tumor viruses: human papillomaviruses (HPVs) and Merkel cell polyomavirus (MCPyV). The study of small DNA tumor viruses (adenoviruses, polyomaviruses, and papillomaviruses) has facilitated several significant biological discoveries and established some of the first animal models of virus-associated cancers. The development and use of preclinical in vivo models to study HPVs and MCPyV and their role in human cancer is the focus of this review. Important considerations in the design of animal models of small DNA tumor virus infection and disease, including host range, cell tropism, choice of virus isolates, and the ability to recapitulate human disease, are presented. The types of infection-based and transgenic model strategies that are used to study HPVs and MCPyV, including their strengths and limitations, are also discussed. An overview of the current models that exist to study HPV and MCPyV infection and neoplastic disease are highlighted. These comparative models provide valuable platforms to study various aspects of virus-associated human disease and will continue to expand knowledge of human tumor viruses and their relationship with their hosts.
Topics: Animals; Humans; Merkel cell polyomavirus; Polyomavirus Infections; Tumor Virus Infections; Neoplasms; Polyomavirus; Oncogenic Viruses
PubMed: 35636683
DOI: 10.1016/j.tvr.2022.200239 -
Current Opinion in Immunology Oct 2021Oncoviruses are viruses that can cause tumors. Seven viruses are currently recognized as oncogenic in humans: Epstein Barr virus (EBV), Kaposi sarcoma-associated... (Review)
Review
Oncoviruses are viruses that can cause tumors. Seven viruses are currently recognized as oncogenic in humans: Epstein Barr virus (EBV), Kaposi sarcoma-associated herpesvirus (KSHV, also known as HHV8), human papillomaviruses (HPVs), hepatitis B virus (HBV), hepatitis C virus (HCV), human T-lymphotropic virus-1 (HTLV-1), and Merkel cell polyomavirus (MCPyV). The clinical phenotypes resulting from infection with these oncoviruses range from asymptomatic infection to invasive cancers. Patients with inborn errors of immunity (IEI) are prone to the development of infectious diseases caused by a narrow or broad spectrum of pathogens, including oncoviruses in some cases. Studies of patients with IEI have deepened our understanding of the non-redundant mechanisms underlying the control of EBV, HHV8 and HPV infections. The human genetic factors conferring predisposition to oncogenic HBV, HCV, HTLV-1 and MCPyV manifestations remain elusive. We briefly review here what is currently known about the IEI conferring predisposition to severe infection with oncoviruses.
Topics: Autoimmunity; Biomarkers; Genetic Predisposition to Disease; Genetic Variation; Host-Pathogen Interactions; Humans; Immunity; Mutation; Oncogenic Viruses; Phenotype; Species Specificity; Tumor Virus Infections
PubMed: 34364035
DOI: 10.1016/j.coi.2021.06.017 -
Viruses Jul 2021Insulin-like growth factor-1 (IGF-1) and the IGF-1 receptor (IGF-1R) belong to the insulin-like growth factor family, and IGF-1 activates intracellular signaling... (Review)
Review
Insulin-like growth factor-1 (IGF-1) and the IGF-1 receptor (IGF-1R) belong to the insulin-like growth factor family, and IGF-1 activates intracellular signaling pathways by binding specifically to IGF-1R. The interaction between IGF-1 and IGF-1R transmits a signal through a number of intracellular substrates, including the insulin receptor substrate (IRS) and the Src homology collagen (Shc) proteins, which activate two major intracellular signaling pathways: the phosphatidylinositol 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK) pathways, specifically the extracellular signal-regulated kinase (ERK) pathways. The PI3K/AKT kinase pathway regulates a variety of cellular processes, including cell proliferation and apoptosis. IGF1/IGF-1R signaling also promotes cell differentiation and proliferation via the Ras/MAPK pathway. Moreover, upon IGF-1R activation of the IRS and Shc adaptor proteins, Shc stimulates Raf through the GTPase Ras to activate the MAPKs ERK1 and ERK2, phosphorylate and several other proteins, and to stimulate cell proliferation. The IGF-1 signaling pathway is required for certain viral effects in oncogenic progression and may be induced as an effect of viral infection. The mechanisms of IGF signaling in animal viral infections need to be clarified, mainly because they are involved in multifactorial signaling pathways. The aim of this review is to summarize the current data obtained from virological studies and to increase our understanding of the complex role of the IGF-1 signaling axis in animal virus infections.
Topics: Animals; Humans; Insulin-Like Growth Factor I; Mice; Oncogenic Viruses; Phosphorylation; Receptor, IGF Type 1; Signal Transduction; Virus Diseases
PubMed: 34452353
DOI: 10.3390/v13081488 -
Viruses Dec 2019Viral lymphomagenesis induced by infection with oncogenic viruses, such as Kaposi's sarcoma associated herpesvirus (KSHV), Epstein-Barr virus (EBV) and human T-cell... (Review)
Review
Viral lymphomagenesis induced by infection with oncogenic viruses, such as Kaposi's sarcoma associated herpesvirus (KSHV), Epstein-Barr virus (EBV) and human T-cell leukemia virus (HTLV-1), represents a group of aggressive malignancies with a diverse range of pathological features. Combined chemotherapy remains the standard of care for these virus-associated lymphomas; however, frequent chemoresistance is a barrier to achieving successful long-term disease-free survival. There is increasing evidence that indicates virus-associated lymphomas display more resistance to cytotoxic chemotherapeutic agents than that observed in solid tumors. Although the tumor microenvironment and genetic changes, such as key oncogene mutations, are closely related to chemoresistance, some studies demonstrate that the components of oncogenic viruses themselves play pivotal roles in the multidrug chemoresistance of lymphoma cells. In this review, we summarize recent advances in the understanding of the mechanisms through which oncogenic viruses mediate lymphoma cell chemoresistance, with a particular focus on KSHV and EBV, two major oncogenic viruses. We also discuss the current challenges to overcome these obstacles in the treatment of virus-associated lymphomas.
Topics: Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Cell Line, Tumor; Drug Resistance, Neoplasm; Epstein-Barr Virus Infections; Herpesvirus 4, Human; Humans; Lymphoma; Oncogenic Viruses; Tumor Virus Infections
PubMed: 31888174
DOI: 10.3390/v11121161 -
Viruses Oct 2014The first human tumor virus was discovered in the middle of the last century by Anthony Epstein, Bert Achong and Yvonne Barr in African pediatric patients with Burkitt's... (Review)
Review
The first human tumor virus was discovered in the middle of the last century by Anthony Epstein, Bert Achong and Yvonne Barr in African pediatric patients with Burkitt's lymphoma. To date, seven viruses -EBV, KSHV, high-risk HPV, MCPV, HBV, HCV and HTLV1- have been consistently linked to different types of human cancer, and infections are estimated to account for up to 20% of all cancer cases worldwide. Viral oncogenic mechanisms generally include: generation of genomic instability, increase in the rate of cell proliferation, resistance to apoptosis, alterations in DNA repair mechanisms and cell polarity changes, which often coexist with evasion mechanisms of the antiviral immune response. Viral agents also indirectly contribute to the development of cancer mainly through immunosuppression or chronic inflammation, but also through chronic antigenic stimulation. There is also evidence that viruses can modulate the malignant properties of an established tumor. In the present work, causation criteria for viruses and cancer will be described, as well as the viral agents that comply with these criteria in human tumors, their epidemiological and biological characteristics, the molecular mechanisms by which they induce cellular transformation and their associated cancers.
Topics: Apoptosis; Cell Transformation, Neoplastic; Genomic Instability; Humans; Immune Tolerance; Neoplasms; Oncogenic Viruses; Tumor Virus Infections
PubMed: 25341666
DOI: 10.3390/v6104047 -
Viruses Mar 2024Approximately 12% of human cancers worldwide are associated with infectious agents, which are classified by the International Agency for Research on Cancer (IARC) as... (Review)
Review
Approximately 12% of human cancers worldwide are associated with infectious agents, which are classified by the International Agency for Research on Cancer (IARC) as Group 1 within the agents that are carcinogenic to humans. Most of these agents are viruses. Group 1 oncogenic viruses include hepatitis C virus, hepatitis B virus (HBV), human T-cell lymphotropic virus type 1, Epstein-Barr virus, Kaposi sarcoma-associated herpesvirus, human immunodeficiency virus-1 and high-risk human papillomaviruses (HPVs). In addition, some human polyomaviruses are suspected of inducing cancer prevalently in hosts with impaired immune responses. Merkel cell polyomavirus has been associated with Merkel cell carcinoma and included by the IARC in Group 2A (i.e., probably carcinogenic to humans). Linking viruses to human cancers has allowed for the development of diagnostic, prophylactic and therapeutic measures. Vaccination significantly reduced tumours induced by two oncogenic viruses as follows: HBV and HPV. Herein, we focus on mucosal alpha HPVs, which are responsible for the highest number of cancer cases due to tumour viruses and against which effective prevention strategies have been developed to reduce the global burden of HPV-related cancers.
Topics: Humans; Oncogenic Viruses; Human Papillomavirus Viruses; Papillomavirus Infections; Epstein-Barr Virus Infections; Herpesvirus 4, Human; Neoplasms; Viruses; Carcinogenesis; Hepatitis B virus
PubMed: 38543781
DOI: 10.3390/v16030416 -
Biomedicine & Pharmacotherapy =... Oct 2021To date, seven viruses have been reliably connected to various forms of human cancer: Epstein Barr Virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), high-risk... (Review)
Review
To date, seven viruses have been reliably connected to various forms of human cancer: Epstein Barr Virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), high-risk Human papillomavirus (HPV), Merkel Cell Polyomavirus (MCPV), Hepatitis B virus (HBV), hepatitis C virus (HCV), and Human T-cell leukemia virus type 1 (HTLV1). This mini-review summarizes two of these viruses, EPV and HTLV-1, in terms of their general pathway of infection, the key mechanism of cancer induction, and the prominent technologies used to detect the infections. EBV is the first discovered human oncovirus and HTLV - I is the first human retrovirus and both were discovered from patient with distinct lymphoma clinical condition. Both the viruses can immortalize lymphocytes invitro and lymphomas are common manifestation of majority oncogenic viruses. Lymphomagenesis are discovered in associated with EBV, HTLV-I, Human Immunodeficiency virus (HIV), Kaposi sarcoma - associated herpes virus and hepatitis c virus. Later the undefined mechanism behind the induction of cancer by these viruses was unveiled gradually along with the responsible cofactors and mimicry mechanism. These two viruses contrast in their genetic structure, location of the infection, and latency, yet clinically, they generate similar cancer disorders. The major focus of this study is to brief the mechanism of these two unrelated viral cancer promoting agents on how they simulate a condition similar to lymphoma which may or may not undergo mimicry and cofactor utilization process, handpicked and vital genes behind the transformation mechanism are given accordingly.
Topics: Carcinogenesis; Epstein-Barr Virus Infections; HTLV-I Infections; Herpesvirus 4, Human; Human T-lymphotropic virus 1; Humans; Neoplasms
PubMed: 34343895
DOI: 10.1016/j.biopha.2021.111974 -
Biochemistry. Biokhimiia Oct 2020The disruption of apoptotic cell death process is closely associated with the etiology of various diseases, including cancer. Permanent viral infections can cause... (Review)
Review
The disruption of apoptotic cell death process is closely associated with the etiology of various diseases, including cancer. Permanent viral infections can cause different types of cancers. Oncogenic viruses manipulate both external and internal apoptosis pathways, and inhibit the activity of proapoptotic proteins and signaling pathways, which facilitates carcinogenesis. Ineffective immune surveillance or immune response suppression can induce uncontrolled virus propagation and host cell proliferation. In this review, we discuss current data that provide insights into mechanisms of apoptotic death suppression by viruses and their role in oncogenesis.
Topics: Apoptosis; Carcinogenesis; Cell Line, Tumor; Gene Expression Regulation; Humans; Mitochondria; NF-kappa B; Oncogenic Viruses; Phosphatidylinositol 3-Kinases; Tumor Suppressor Protein p53; Tumor Virus Infections
PubMed: 33202204
DOI: 10.1134/S0006297920100077 -
Current Opinion in Virology Dec 2019Oncogenic viruses, like all viruses, relies on host metabolism to provide the metabolites and energy needed for virus replication. Many DNA tumor viruses and... (Review)
Review
Oncogenic viruses, like all viruses, relies on host metabolism to provide the metabolites and energy needed for virus replication. Many DNA tumor viruses and retroviruses will reprogram metabolism during infection. Additionally, some viral oncogenes may alter metabolism independent of virus replication. Virus infection and cancer development share many similarities regarding metabolic reprogramming as both processes demand increased metabolic activity to produce biomass: cell proliferation in the case of cancer and virion production in the case of infection. This review discusses the parallels in metabolic reprogramming between human oncogenic viruses and oncogenesis.
Topics: Biomass; Carcinogenesis; Cell Proliferation; Cellular Reprogramming; Hepacivirus; Hepatitis B virus; Herpesviridae; Humans; Merkel cell polyomavirus; Metabolic Networks and Pathways; Neoplasms; Oncogenic Viruses; Papillomaviridae; Retroviridae; Virion; Virus Replication
PubMed: 31766001
DOI: 10.1016/j.coviro.2019.11.002